Q1.3: What is the mechanism of LTP (e.g., neurochemistry, effects on specific ion-channels related to transmitter release, etc.) - specifically in synapses located in a part of the brain relevant to AD?

Q1.4: Would an antibody directed against ADDL / Abeta*56 restore A-current in the mouse model hippocampal neuron (e.g. in an organotypic slice prep)?

Q2: What determines vulnerability to encephalilitis among ADDL immunized patients?

Q2.1: Do polymorphisms in INFG, or differences in INFG regulation, correlate with inflammatory response to ADDL vaccine?

Q2.2: Why did the mouse models not develop encephalitis in preclinical studies?

A2.2: Query of SNP databases for differences between mouse strains, mouse and human. He narrows down a group of genes and queries the AlzGene database to see if any gene association studies have shown a correlation between any of these genes and AD risk.

Result:

Our investigator proposes a study to genotype participants in the failed vaccination trial to find out whether the encephalitis response correlates with specific SNPs in the candidate genes.